Endometriosis is a chronic gynecological disorder characterized by ectopic endometrial growth, inflammation, and mitochondrial dysfunction within the cumulus–oocyte complex (COC), leading to impaired oocyte competence. Truncated BID (tBID) plays a central role in linking extrinsic and intrinsic apoptotic pathways, and its dysregulation contributes to mitochondrial-mediated apoptosis in endometriosis. Curcumin possesses anti-inflammatory and anti-apoptotic properties; however, its limited bioavailability may be enhanced through nanoparticle formulation as nanocurcumin. This study aimed to evaluate the effect of nanocurcumin on tBID expression in an experimental endometriosis model. Thirty-one female Mus musculus were randomly assigned into four groups: positive control (C+) and three treatment groups receiving oral nanocurcumin at 2.5 mg/kgBW (T1), 5 mg/kgBW (T2), and 10 mg/kgBW (T3) for 14 days. Ovarian tissues were collected, and tBID expression in granulosa cells was assessed by immunohistochemistry and semi-quantified using the Immunoreactive Score (IRS). All animals developed endometriosis features. Nanocurcumin treatment significantly reduced tBID expression compared with the control group (p < 0.05), with the lowest expression observed in T3 (IRS 1.57 ± 0.26). Post hoc analysis demonstrated a dose-dependent reduction, with T3 differing significantly from T1 and the control. These findings indicate that nanocurcumin downregulates tBID expression, suggesting attenuation of mitochondrial-mediated apoptosis and potential preservation of oocyte quality in endometriosis. This study supports the therapeutic potential of nanocurcumin as a non-hormonal adjuvant for endometriosis, in line with Sustainable Development Goal 3 (Good Health and Well-being), particularly in addressing reproductive health challenges in women. Keywords: Endometriosis, Nanocurcumin, Truncated BID, Cumulus–Oocyte Complex, Good Health and Well-being.
Widyanugraha et al. (Wed,) studied this question.